Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways

• DOI: 10.1016/j.jgr.2015.09.005
• Publication Date: 2015-10-25T07:58:51Z
• Authors: Na Qin; Wei Yang; Dongxu Feng; Xinwen Wang; Muyao Qi; Tianxin Du; Hongzhi Sun; Shufang Wu
• Keywords: cGMP-dependent protein kinase; Right ventricular hypertrophy

Ginsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension elucidate underlying mechanism.MCT-intoxicated rats were treated with gradient doses of TG, or without N (G)-nitro-l-arginine methyl ester. The levels molecules involving regulation nitric oxide mitogen-activated protein kinase pathways determined.TG ameliorated MCT-induced in a dose-dependent manner, as assessed by right ventricular systolic pressure, hypertrophy index, arterial remodeling. Furthermore, TG increased oxide, endothelial synthase, cyclic guanosine monophosphate. Lastly, phosphatase-1 expression promoted dephosphorylation extracellular signal-regulated kinases 1/2, p38 kinase, c-Jun NH2-terminal 1/2.TG attenuates hypertension, which may involve part pathways.